Abstract
In this study, we examined modulations in phosphatase and tensin homolog (PTEN) and mammalian target of rapamycin (mTOR) protein expression after a lateral C2 hemisection and subsequent intermittent hypoxia (IH) exposure and training, which initiates respiratory motor plasticity and recovery. PTEN and mTOR are significant molecules within a signaling pathway that directly influences dendritic sprouting, axonal plasticity, and regeneration. Expression levels of PTEN, mTOR and downstream effectors within this pathway were investigated, and it was found that following injury and IH exposure the expression of these molecules was significantly altered. This study directly demonstrates the implementation and feasibility of a non-invasive strategy to modulate the expression levels of intrinsic signaling molecules known to influence plasticity and regeneration in the CNS.
Original language | English |
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Pages (from-to) | 45-52 |
Number of pages | 8 |
Journal | Experimental Neurology |
Volume | 248 |
DOIs | |
State | Published - Oct 2013 |
Bibliographical note
Funding Information:This work was supported by grants to WJA from the International Spinal Research Trust in the UK and the Craig H. Neilsen Foundation . Additional support comes from MetroHealth Medical Center in Cleveland, Ohio . We also acknowledge Drs. Philippa Warren and Kevin Hoye for providing constructive insight about data presentation and statistical guidance. Additional thanks to Dr. Diana Kunze for allowing us to use her intermittent hypoxia chambers.
Keywords
- Breathing
- Intermittent hypoxia
- MTOR
- PTEN
- Phrenic motor neurons
- Plasticity
- Spinal cord injury
ASJC Scopus subject areas
- Neurology
- Developmental Neuroscience